In ovarian cancer in particular, Stone et al. [243] demonstrated while using preclinical in vivo models that combining DNMT inhibitor and HDAC inhibitor with immune checkpoint blockade resulted in the most notable anti-cancer effect and survival due to activation of type I interferon signaling, more efficient recruitment of anti-tumor TIL subsets and the restriction of tumor-indulgent TAMs and myeloid-derived suppressor cells to the ovarian TME. This evidence concerns the gene HDAC9 and neoplasm.